College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi 710119 China.
College of Life Sciences, Shaanxi Normal University, Xi'an, Shaanxi 710119 China.
Ecotoxicol Environ Saf. 2018 Nov 30;164:500-509. doi: 10.1016/j.ecoenv.2018.08.058. Epub 2018 Aug 23.
Mercury is severely detrimental to organisms and is ubiquitous in both terrestrial and aquatic ecosystems. In the present study, we examined the effects of chronic mercury (Hg) exposure on metamorphosis, body size, thyroid microstructures, liver microstructural and ultrastructural features, and transcript levels of genes associated with lipid metabolism, oxidative stress and thyroid hormones signaling pathways of Chinese toad (Bufo gargarizans) tadpoles. Tadpoles were exposed to mercury concentrations at 0, 6, 12, 18, 24 and 30 µg/L from Gosner stage 26-42 of metamorphic climax. The present results showed that high dose mercury (24 and 30 µg/L) decelerated metamorphosis rate and inhibited body size of B. gargarizans larvae. Histological examinations have clearly exhibited that high mercury concentrations caused thyroid gland and liver damages. Moreover, degeneration and disintegration of hepatocytes, mitochondrial vacuolation, and endoplasmic reticulum breakdown were visible in the ultrastructure of liver after high dose mercury treatment. Furthermore, the larvae exposed to high dose mercury demonstrated a significant decrease in type II iodothyronine deiodinase (Dio2) and thyroid hormone receptor α and β (TRα and TRβ) mRNA levels. Transcript level of superoxide dismutase (SOD) and heat shock protein (HSP) were significantly up regulated in larvae exposed to high dose mercury, while transcript level of phospholipid hydroperoxide glutathione peroxidase (PHGPx) was significantly down regulated. Moreover, exposure to high dose mercury significantly down regulated mRNA expression of carnitine palmitoyltransferase (CPT), sterol carrier protein (SCP), acyl-CoA oxidase (ACOX) and peroxisome proliferator-activated receptor α (PPAPα), but significantly up regulated mRNA expression of fatty acid elongase (FAE), fatty acid synthetase (FAS) and Acetyl CoA Carboxylase (ACC). Therefore, we conclude that high dose mercury induced thyroid function disruption, liver oxidative stress and lipid metabolism disorder by damaging thyroid and liver cell structures and altering the expression levels of relevant genes.
汞对生物体有严重的危害，在陆地和水生生态系统中普遍存在。在本研究中，我们研究了慢性汞（Hg）暴露对中国蟾蜍（Bufo gargarizans）蝌蚪变态、体型、甲状腺微观结构、肝脏微观和超微结构特征以及与脂质代谢、氧化应激和甲状腺激素信号通路相关基因转录水平的影响。从变态高峰期的 Gosner 阶段 26-42 开始，将蝌蚪暴露于 0、6、12、18、24 和 30μg/L 的汞浓度下。结果表明，高剂量汞（24 和 30μg/L）减缓了变态率并抑制了 B. gargarizans 幼虫的体型。组织学检查清楚地表明，高浓度的汞会导致甲状腺和肝脏受损。此外，在高剂量汞处理后，肝细胞出现退化和崩解、线粒体空泡化和内质网破裂等现象。此外，暴露于高剂量汞的幼虫中，II 型碘甲状腺原氨酸脱碘酶（Dio2）和甲状腺激素受体 α 和 β（TRα 和 TRβ）mRNA 水平显著降低。暴露于高剂量汞的幼虫中超氧化物歧化酶（SOD）和热休克蛋白（HSP）的转录水平显著上调，而磷脂氢过氧化物谷胱甘肽过氧化物酶（PHGPx）的转录水平显著下调。此外，暴露于高剂量汞显著下调了肉碱棕榈酰转移酶（CPT）、固醇载体蛋白（SCP）、酰基辅酶 A 氧化酶（ACOX）和过氧化物酶体增殖物激活受体α（PPAPα）的 mRNA 表达，而脂肪酸延长酶（FAE）、脂肪酸合成酶（FAS）和乙酰辅酶 A 羧化酶（ACC）的 mRNA 表达显著上调。因此，我们得出结论，高剂量汞通过破坏甲状腺和肝细胞结构以及改变相关基因的表达水平，导致甲状腺功能障碍、肝脏氧化应激和脂质代谢紊乱。
